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BMS200 final exam > Week 11 > Flashcards

Week 11 Flashcards

1
Q

what gets exposed when blood vessel is injured

A

collagen and thromboplastin

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2
Q

platelets release 5-hydroxytrptamine ofr

A

muscle contraction + vasoconstriction

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3
Q

extrinsic vs intrinsic pathway; which is first

A

extrinsic first and form early fibrin plug

intrinsic to amplify coagulation and make stable fibrin plug

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4
Q

what activates fibrinogen to fibrin

A

thrombin

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5
Q

antithomrobotic factors (prevent clot formation)

A

prostacyclin, NO, ADPase

heparan sulfate
protein C

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6
Q

where are platelets made

A

megakaryotcytes in bone marrow

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7
Q

what regulates platelet production in the marrow

A

thrombopoietin

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8
Q

what increased platelet production

A

IL6 (inflammation) and decreased platelet numbers

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9
Q

lifespan of platelet

A

7-10 days

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10
Q

where are platelets stored

A

spleen

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11
Q

2 types of granules in platelets (which is most abundant)

A

alpha granules (most abundant) and dense granules

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12
Q

dense granules in platelets contain

A

ADP, Ca2+, serotonin, polyphosphate

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13
Q

alpha granules in platelets contain

A

vWF, FV, fibrinogen, growth factors (FGF, VEGF, PDGF), adhesive glycoproteins

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14
Q

which granule in platelet has adhesive glycoproteins to help bind injury

A

alpha granules

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15
Q

platelet glycoproteins in alpha granules

A

GP Ib/IX binds vWF

GP Ia/IIa binds collagen

these 2 above are for initial signals

GPIIb/IIIa- binds fibrinogen or vWF (only after platelet activates it by plateRR) (stabilize plug- platelet aggregation)

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16
Q

healthy endothelium contains _____ to prevent platelet activation

A

NO, prostacyclin, ADPase

vWF and collagen are hidden

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17
Q

plateRR (release reaction) releases many things to help clot

A

ADP, serotonin, thromboxane A2, coagulation factors, Ca2+, polyphosphate

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18
Q

how to platelets get leukocyte to injury

A

express P selectin

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19
Q

1st step in intrinsic and extrinsic pathway and final common pathway

A

extrinsic: FVIIa and TF (aka TPL or thromboplastin)

intrinsic: HMW kinongen kallikrein with FXIIa to activate

final: FXa + FVa + Ca2+ –> activate thrombin

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20
Q

what factor stabilizes fibrin

A

XIIIa

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21
Q

what does kinin-kvllikrein system release

A

bradykinin (vasodilate, pain, muscle contract, permeability)

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22
Q

FXII in intrinsic pathway causes inflammation via

A

bradykinin release

C3 and C5 cleavage

thrombin and fibrin split products (clot left overs)

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23
Q

decrease clot formation by

A

down regulate platelet activation (prostacyclin, NO, ADPase)

down regulate coagulation cascade

destroy clots (fibrinolysis)

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24
Q

antithrombotic/ anticoagulation mechanisms (stop clotting)

A
  • antithrombin via heparin expression

protein C + protein S = thrombomodulin

tissue factor pathway inhibitor (TFPI) via heparin

plasminogen –> plasmin

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25
fibrinolysis how does plasminogen become plasmin? how does it degrade fibrin? into what?
plasminogen into plasmin via tPA (tissue plasminogen activator) and its degrades fibers into d -dimers
26
how to stop plasminogen from turning into plasmin and causing fibrinolysis (this is if you want clots)
plasminogen activator inhibitors (PAIs) block tPA
27
prothrombin time (PT) vs activated partial thromboplastin time (aPTT) - which is for extrinsic vs intrinsic pathway
PT= extrinsic aPTT= intrinsic
28
hemophilia A vs B deficiency in which factors
A= FVIII (8) B=FIX (9) both are x linked recessive + similar clinical presentation
29
whats more common, hemophilia A or B
A
30
hemophilia presentation
deep bleeds in soft tissue... cant clot
31
RBCs/ erythrocytes are made in _____ (lifespan of _____) and recycled in _____
Red blood cells are produced in the bone marrow and have a lifespan of about 120 days (because no nucleus) before being recycled in the liver and spleen.
32
hemoglobin binds oxygen with low or high oxygen concentrations?
* Hb binds to oxygen at high oxygen concentrations * Oxygen dissociates from Hb at low oxygen concentrations
33
RBCs bind CO2 with what enzyme and converts it into what
carbonic anhydrase enzyme and converts it into bicarbonate ions (HCO3-)
34
what are RBCs derived from
myeloid progenitor (pronormoblast)
35
myeloid progenitor (pronormoblast) divide to become RBC via what
GM-CSF and EPO (erythropoietin)
36
erythropoiesis
pronormoblast divide to make 16-32 RBC via EPO
37
low O2 or high O2 to make EPO
low oxygen to make EPO high oxygen HIF (hypoxia inducible factor) degrades EPO
38
which energy for RBC to make ATP
glycolysis (no mitochondria)
39
what is stored in RBC to protect against free radicals and oxidative stress when high oxygen concentrations
glutathione
40
hemoglobin composition
2 alpha + 2 other mostly 2 beta sometimes delta fetal is gamma
41
what causes Hb to have a lower affinity for oxygen (less binding)
increase temp, increase DPG, increase CO2, decrease pH
42
what has greater affinity for Hb than oxygen
CO2
43
where are RBCs eliminated
red pulp is spleen
44
Hb metabolism
iron sent back to bone marrow for storage heme elimintated in stool and bile as bilirubin (via biliverdin --> unconjugated bilirubin bound to albumin and carried to liver) (UDG catalyzes conjugation of bilirubin) globin protein recycled back into a.a. components
45
what catalyzed conjugation of bilirubin when gets to liver
add glucoronic acid residues via UDG (uridine diphosphate glucosyntransferase)
46
what forms of iron are better absorbed
heme (animal) Fe2+ (reduced)h
47
how to transport iron
divalent metal transporter (DMT)
48
what blocks ferroportin transporter (for iron inside the cell to get extracellular)
hepcidin - prevent iron overload
49
what transports iron through bloodstream
transferrin (accepts iron from ferroportin)
50
ferritin is
from when cells with transferring receptors endocytose it
51
what prevents iron overload
hepcidin (block ferroportin)
52
what is the storage form of ferritin in hepatocytes, spleen, bone marrow
hemosiderin
53
what stimulates hepcidin production
IL6
54
what inhibits hepcidin (something that prevents iron overload)
-reduced iron stores -erythroferrone (released from developing erythroblasts)
55
IDA
microcytic + hypochromic (decreased MCHC) increased RDW, TIBC decrease HB, RBC count, reticulocytes, ferritin
56
what values are sensitive to early iron store depletion
Measurements of marrow iron stores, serum ferritin, and total iron-binding capacity (TIBC) are sensitive to early iron- store depletion
57
absolute iron deficiency vs functional iron deficiency
absolute: Reduction of total body iron stores, which may progress to IDA. (i.e. increased demand, decrease intake and absorption, chronic blood loss) functional: Iron is inadequately mobilized from stores to the circulation and erythropoietic tissue. (I.e. chronic inflammation and elevated hepcidin, increased erythropoiesis)
58
anemias of inflammation differ from IDA
▪ Present similarly and have similar findings on CBC ▪ Iron handling is quite different
59
in anemias of inflammation what cytokines suppress erythropoiesis
rheumatoid arthritis: IL-1 neoplasm, baterial infection: TNF
60
inflammatory cytokines (IL1 and TNF alpha) do what do erythropoeisis
suppress it (EPO)
61
what suppresses RBC precurors in anemais of inflammation
IFNs (IFN release is stimulated by TNF and IL1)
62
IL1 and TNF alpha stimulate release of ____ which increases the production of _____
IL6 to produce hepcidin (which decreases iron)
63
anemia of chronic kidney disease
hypo proliferative anemia (not make enough RBC from bone marrow) from decreased EPO and poor RBC survival
64
RBCs in chronic kidney disease
normocytic and normochromic
65
RBC in anemia of inflammation
normochromic and mildly microcytic decrease reticulocytes (immature RBCs)
66
hereditary spherocytosis
anemia from defects in cytoskeletal elements (make abnormal shaped RBCs- spherocytes; so get destroyed)
67
genetic mutations in hereditary spherocytosis
ankryin and anion exchanger 1
68
symptoms in hereditary spherocytosis
splenomegaly, jaundice normoctyic anemia, increase RDW and MCHC
69
G6PD deficiency how does G6PD play a role in RBC
source of NADPH for glutathione reduction
70
when do G6PD deficiency symptoms arise
in oxidative stress bc related to NADPH and glutathione
71
type of anemia in G6PD deficiency
Hemolytic anemia precipitated by oxidative insults to RBCs
72
Alpha and beta thalassemia
reduce adult haemoglobin synthesis alpha- deficit in alpha globin chain production (more fatal) beta- defect in beta globin chain production defects lead to wrong shape and poor RBC production (ineffective erythroposeis) --> increased RBC destruction (hemolysis)
73
if give blood transfusion to thalassemia
can help with anemia but then can cause iron overload (the iron levels are normal its just the hemoglobin that's low)
74
types of beta thalassemia
minor: microcytic anemia intermedia: need transfusions major (both alleles): splenomegaly, bone deformities
75
4 missing alpha chains for alpha thalasemia is aka
hydros fetalis (fatal)
76
3 missing alpha chains in thalassemia
hemoglobin H disease microytci hypochromic anemia, splenomegaly
77
sickle cell disease
replace glutamate with valine at codon 6 of beta-globin gene for malaria protection sickling damages RBCs and leads to their removal and micro infarcts hypoxia
78
type of anemia in sickle cell
hemolytic anemia
79
bug that causes malaria
female anopheles mosquitos carrying the p. falciparum parasite invade the liver then get into blood
80
what does malaria induce RBCs to express on their membrane
Malaria induces RBCs to express a parasitic protein on their membrane – PfEMP1 makes them get stuck in vasculature
81
bad malaria effects
hypoglycemia, convulsions, renal failure, if cerebral , acidosis,
82
leukemia vs lymphoma
leuk- bone marrow lymphoma- lymphatics (can invade bone marrow)
83
lymphoid neoplasms in which cells most common and which enzymes
B cell precursors (malignancies develop during antibody class switching and recombination events) Enzymes (AID = activation-induced cytosine deaminase and recombinases/RAGs
84
non-hodkin vs hodgkin lymphoma
hod- along lymphs non- widespread
85
acute lymphoblastic leukemia
b and T cell precursors in kids block differentiation of immature leukemic blast cells immature non functional blast cells accumulate crowd out normal cells and bone marrow fails
86
chronić lymphocytic leukemia
Tumour of relatively mature B-cells, expressing CD 19, CD 20, and CD 23
87
acute lymphoblastic leukemia vs chronic lymphocytic leukemia
acute-b and T cell precursors chronic- Tumour of relatively mature B-cells, expressing CD 19, CD 20, and CD 23
88
non Hodgkins lymphoma
Cancers of mature B, T, and NK cells. ( B cell most common)
89
mutations in which transcription factors to get B cell type of non-hodgkins lymphoma
transcription factors MYC and BCL6, and antiapoptotic protein BCL2.
90
Hopkins lymphoma affects
matter B cells
91
2 types of Hodgkins lymphoma
classical Hodgkin's lymphoma (cHL) and nodular lymphocyte-predominant Hodgkin's lymphoma (NLPHL).
92
association between what a Hodgkin lymphoma
Epstein barr virus , HIV too
93
type of cells in Hodgkin lymphoma
reed-stern berg cells (large cells with abdundant cytoplasm and multiple nuclei), express EBV protein

BMS200 final exam (14 decks)

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